Risk stratification is an essential part of appropriately informing patients electing to undergo percutaneous coronary intervention or coronary artery bypass graft surgery. In addition, there is a greater need than ever to tailor revascularization appropriately, taking into consideration a patient's co-morbidities, coronary anatomy, personal preferences, and individual perception of risk. This chapter examines the important established and evolving contemporary clinical tools used to aid the Heart Team in this risk-stratification process. Risk scores based on clinical and anatomical variables alone and in combination are all explored. Other areas of discussion include risk scores based upon completeness of revascularization and decision-making between surgical and percutaneous-based revascularization in complex coronary artery disease.
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There is a pressing need for more effective drug treatments for COPD. New bronchodilators include a long-acting anticholinergic tiotropium bromide and a dual beta2-dopamine2-receptor agonist. But no treatments prevent the progression of COPD. Mediator antagonists in development include leukotriene B4 antagonists, chemokine receptor antagonists and more potent antioxidants. The inflammation of COPD is resistant to corticosteroids, so new anti-inflammatory drugs need to be developed. These include phosphodiesterase-4 inhibitors, nuclear factor-kappaB inhibitors and p38 MAP kinase inhibitors. Small molecule protease inhibitors, including neutrophil elastase inhibitors and selective matrix metalloproteinase inhibitors are also in development. Future drug targets may be identified by gene array and proteomics.
A 62-year-old woman with an 8-year history of hypertrophic cardiomyopathy and recent septal myotomy and/or myectomy underwent simultaneous hemodynamic and two-dimensional and Doppler echocardiographic evaluation. Evidence of abnormal diastolic relaxation in the absence of obstruction or systolic cavity obliteration was observed. Two abnormal patterns of diastolic blood flow were detected: flow from the left ventricular outflow tract toward the left ventricular body during isovolumetric relaxation, and middiastolic blood flow from the left ventricular body toward the mitral apparatus. This case provides evidence of abnormal diastolic function and two patterns of abnormal diastolic blood flow in a patient with hypertrophic cardiomyopathy but without a systolic gradient or cavity obliteration. These findings support the importance of disturbed diastolic function in the pathogenesis of hypertrophic cardiomyopathy.
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